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Microplastics drives ILC2s function and fatty acid metabolism in allergic airway inflammation via PPARγ signaling
Summary
Researchers found that microplastics exacerbate allergic airway inflammation in house dust mite-sensitized mice by promoting epithelial barrier disruption and type 2 immune activation. The study revealed that microplastics drive the function of innate lymphoid cells (ILC2s) and alter fatty acid metabolism through the PPARgamma signaling pathway, providing mechanistic insight into how airborne microplastics may worsen respiratory allergies.
Microplastics (MPs), emerging airborne pollutants detected in human lungs, are increasingly recognized as potential drivers of respiratory disease, yet their roles and pathogenic mechanisms in allergic airway inflammation remain poorly understood. Here we show that MPs exacerbate allergic airway inflammation in house dust mite (HDM)-sensitized mice by promoting epithelial barrier disruption and type 2 immune activation. MPs exposure elevated IL-33 release and expanded IL-5⁺IL-13⁺ ILC2s. Mechanistically, the Peroxisome proliferator-activated receptor gamma (PPARγ) was markedly expressed in MPs+HDM mice and is highly expressed in ILC2s. In epithelial-ILC2s coculture system, MPs selectively enhanced PPARγ expression in ILC2s, triggering metabolic reprogramming characterized by increased fatty acid uptake and lipid droplet accumulation. This metabolic shift fueled ILC2s activation, cytokine production and downstream ST2 activation, while pharmacological inhibition of PPARγ effectively attenuated these effects. Our findings identify a previously unrecognized epithelial-PPARγ-ILC2s axis through which MPs aggravate allergic airway inflammation, revealing a potential immunometabolic mechanism of MPs-induced lung impairment.